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Lactobacillus plantarum reverse diabetes-induced Fmo3 and ICAM expression in mice through enteric dysbiosis-related

Wen-Chung Liu1,2, Ming-Chieh Yang1,2, Ying-Ying Wu1

  • 1Department of Surgery, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan.

Plos One
|June 1, 2018
PubMed

Insights

Diabetes alters gut bacteria, increasing trimethylamine-N-oxide (TMAO) and promoting atherosclerosis. Correcting gut dysbiosis or inhibiting pJNK can reverse diabetes-induced Fmo3 and ICAM expression, potentially preventing vascular damage.

Area of Science:

  • Metabolic disease research
  • Microbiome studies
  • Vascular biology

Background:

  • Diabetes mellitus (DM) is linked to increased atherosclerosis and fatality.
  • Circulating trimethylamine-N-oxide (TMAO) levels correlate with atherosclerosis severity.
  • The flavin mono-oxygenase family (Fmo) enzymes, particularly Fmo3, metabolize trimethylamine (TMA) to TMAO.

Purpose of the Study:

  • To investigate the role of intestinal microflora in diabetes-induced Fmo3 and intercellular adhesion molecule (ICAM) expression.
  • To elucidate the regulatory mechanisms involving pJNK in these processes.
  • To assess the therapeutic potential of modulating the gut microbiota or inhibiting pJNK.

Main Methods:

  • Utilized streptozotocin-induced diabetic mice (STZDM) and Akita mice (C57BL/6J-Ins2Akita), including JNK1 knockout models.
  • Administered prebiotics (FOS) and probiotics (L. plantarum) to assess reversal of diabetes-induced changes.
  • Analyzed intestinal mucosa, liver, aorta, and serum for markers of inflammation, oxidative stress, Fmo3, and ICAM expression.

Main Results:

  • Diabetic mice showed reduced Lactobacilli, decreased ROS, and increased pJNK, iNOS, IL-1β, and TNF-α.
  • Elevated Fmo3 expression in the liver and ICAM expression in the aorta were observed in diabetic mice.
  • Prebiotic/probiotic treatment and pJNK inhibition normalized these markers, reducing Fmo3 and ICAM levels.

Conclusions:

  • Diabetes-induced enteric dysbiosis contributes to Fmo3 and ICAM upregulation, potentially leading to vascular impairment.
  • Correcting enteric dysbiosis or inhibiting pJNK offers a therapeutic strategy to reverse these diabetes-associated changes.
  • The gut microbiome plays a critical role in mediating the link between diabetes and vascular complications.

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